Outer hair cells are similar to inner hair cells in that they convert sound-induced mechanical vibration into electrical signal as the mechano-sensory cells in the ear. However, outer hair cells also work reciprocally, acting as a fast motor capable of amplifying the mechanical vibration to which these cells respond. These properties of outer hair cells are responsible for the sensitivity and the sharp frequency discrimination of the mammalian ear. We have previously established that the hair cell motor uses electrical energy available at the plasma membrane in a manner similar to piezoelectricity, based on the coupling of electric charge transfer across the membrane with membrane area changes. Specifically, this motility can be reasonably explained by a simple two state model in which two states differ in charge and membrane area. The area difference is determined by tension dependence of the motor activity. However, these observations allowed an alternative motile mechanism that is based on membrane bending.[unreadable] [unreadable] To resolve the issue regarding molecular details of the membrane motor, we examined effects of a sets of chemicals, which bends the plasma membrane by inserting into either external or internal leaf. Those chemicals included chlorpromazine and procaine, which expand the inner leaf, and trinitrophenol and depyridamole, which expand the outer leaf. Despite these two classes of chemicals induce opposite curvature on the plasma membrane, they had similar effects. They all positively shifted the operating point of the cells' voltage dependent motility and shorten the cells. The voltage shifts depended neither on turgor pressure of the cell nor on the presence of the cytoskeleton that underlied the plasma membrane. We found that voltage shifts can be explained by the bending energy of membrane proteins. From those observations we found that the motile mechanism cannot be based on membrane bending but conformational changes of membrane proteins.